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The effect of hole doping on the exchange coupling of the nearest neighbor (NN) Mn pairs in Zn(1-x)MnxTe is probed by inelastic neutron scattering. The difference in the NN exchange energy DeltaJ1 in the presence and in the absence of the holes is determined. The obtained value of DeltaJ1 is in good agreement with the predictions of the Zener/RKKY model, even on the insulator side of the metal-insulator transition.

Limbic event-related potentials related to verbal but not to visual recognition memory have been found to be attenuated within the epileptic hippocampus of patients with temporal lobe epilepsy (TLE). To identify hippocampal contributions to visual processing and memory we recorded intracranial ERPs directly from within the epileptic and the non-epileptic hippocampus in 12 patients with unilateral TLE during a visual object decision and naming task. While the non-epileptic hippocampus differentiated reliably between real and nonsense objects, this effect was completely eliminated within the epileptic mesial temporal lobe. This finding suggests that the hippocampus proper contributes to the semantic processing of visual objects and may help to explain visual memory deficits in TLE.

A variety of involuntary speech phenomena as for example palilalia have been described as consequences of neurological disorders. Palilalia is the involuntary repetition of syllabels, words and phrases in ongoing speech. We describe a 73 year old woman who suffered from a hypertensive thalamic haemorrhage. MRI revealed that the lesion was predominantly located within the pulvinar, extending to the lateroposterior thalamic nuclei and to the pretectal area with possible involvement of the medial geniculate body. Few months after the event she developed involuntary vocalisations with whole words and meaningless syllables being rapidly reiterated. In contrast to typical palilalia these vocalisations were not meaningfully related to the ongoing speech of the patient. In addition, the patient developed a complex hyperkinetic movement disorder with right-sided painful hemidystonia and bilateral clonic jerks and a right-sided postural tremor.

We report on the observation of the Ising quantum Hall ferromagnet with Curie temperature T(C) as high as 2 K in a modulation-doped (Cd,Mn)Te heterostructure. In this system field-induced crossing of Landau levels occurs due to the giant spin-splitting effect. Magnetoresistance data, collected over a wide range of temperatures, magnetic fields, tilt angles, and electron densities, are discussed taking into account both Coulomb electron-electron interactions and s-d coupling to Mn spin fluctuations. The critical behavior of the resistance "spikes" at T-->T(C) corroborates theoretical suggestions that the ferromagnet is destroyed by domain excitations.

A strong influence of illumination and electric bias on the Curie temperature and saturation value of the magnetization is demonstrated for semiconductor structures containing a modulation-doped p-type Cd(0.96)Mn(0.04)Te quantum well placed in various built-in electric fields. It is shown that both light beam and bias voltage generate an isothermal and reversible crossover between the paramagnetic and ferromagnetic phases, in the way that is predetermined by the structure design. The observed behavior is in quantitative agreement with the expectations for systems, in which ferromagnetic interactions are mediated by the weakly disordered two-dimensional hole liquid.

In 1986 Andermann et al. described a syndrome presenting with renal failure, myoclonus, cerebellar symptoms, and epilepsy. They presumed a hereditary cause. We describe the first appearance of this syndrome in Europe, affecting three family members with comparable symptoms. Two of these patients were treated by us, and the third, already decreased, is described according to the available reports. The first clinical symptoms were manifested between the ages of 14 and 20. A female patient suffered from compensated kidney insufficiency and her two brothers aged 18 and 26 required dialysis. Biopsy of kidney tissue revealed nonspecific nephritis. All cases showed a cerebellar syndrome and action myoclonus. Two of them were diagnosed with epilepsy and grand mal seizures, and all suffered from demyelinizing or mixed polyneuropathy. Anamnesis of the family seems to indicate autosomal recessive inheritance.

Ferromagnetism in manganese compound semiconductors not only opens prospects for tailoring magnetic and spin-related phenomena in semiconductors with a precision specific to III-V compounds but also addresses a question about the origin of the magnetic interactions that lead to a Curie temperature (T(C)) as high as 110 K for a manganese concentration of just 5%. Zener's model of ferromagnetism, originally proposed for transition metals in 1950, can explain T(C) of Ga(1-)(x)Mn(x)As and that of its II-VI counterpart Zn(1-)(x)Mn(x)Te and is used to predict materials with T(C) exceeding room temperature, an important step toward semiconductor electronics that use both charge and spin.

Tics-disorders are hyperkinetic movement disorders which manifest in childhood or early adolescence and ameliorate in later adulthood. We report on two patients with a basically subclinical tic-disorder (age of 53 and 68 years). During the therapy of polymyalgia rheumatica and endocrine orbitopathy in Graves disease with prednisolone the tics exacerbated and were therefore diagnosed and treated for the first time. Possible causes for the exacerbation of the tics during the therapy with glucocorticosteroids are discussed in the context of the dopamine hypothesis of tics.

In all mammals investigated so far, an amount of 0.1 - 1 biological unit (KU) of hog pancreatic kallikrein per kg body weight injected intravenously caused a fast reduction in blood pressure with one exception, the rat. Even 1000 times higher doses of hog pancreatic kallikrein did not reduce the blood pressure in this animal. In spite of many experiments performed with rats using hog pancreatic kallikrein to influence various metabolic pathways, there has been no proof, to date, that this enzyme also causes kallikrein-specific effects via kinin liberation in rats. We found only a slow and weak reduction of rat blood pressure after injection of 100 KU hog pancreatic kallikrein per rat, when the endogenous kininases had been previously inactivated by the kininase II inhibitor captopril. However, a fast reduction in blood pressure, similar to the response observed after kinin injection, could be recorded if 90 microliter rat blood, previously incubated for a few minutes with a least 20 k.u. hog pancreatic kallikrein in the presence of captopril, was reinjected. Hence, kinin liberation from rat kininogens by hog pancreatic kallikrein does occur, but proceeds so slowly that the fast kinin degradation by kininases can prevent the typical blood pressure effect of kinin in vivo.

A basic proteinase inhibitor, isoinhibitor K, was purified by SE-Sephadex C-25 column chromatography from the mixture of acid-stable and heat-stable isoinhibitors of the snail (Helix pomatia). Isoinhibitor K is homogeneous in polyacrylamide gel, cellulose acetate and polyacrylamide-dodecylsulfate electrophoresis. From the electrophoretic mobility in dodecylsulfate-polyacrylamide gel and apparent molecular weight of 6500 +/- 200 was estimated. From the amino acid composition the inhibitor consists of 58 amino acid residues. It contains three disulfide bridges, a C-terminal valine and a lysine residue at the reactive site. Isoinhibitor K inhibits the enzymes: bovine trypsin and chymotrypsin, porcine plasmin and pancreatic kallikrein, the trypsin-like component of Streptomyces griseus proteinase-pronase E, and fungi proteinase K from Tritirachium album Limber, which is only inhibited very slightly in contrast to the effect of the mixture of isoinhibitors. The inhibitory effect of isoinhibitor K against these enzymes is compared to that of the mixture or of other isoinhibitors. The following enzymes are not inhibited by isoinhibitor K: Aspergillus proteinase P and alkaline bacillus proteinase 2231 (Röhm), which both are inhibited by the mixture of isoinhibitors. Porcine elastase, bacterial proteinase N (M) (Röhm), and a trypsin-like proteinase from wheat are not inhibited, porcine acrosin and porcine serum kallikrein only to a very minor extent by the mixture of isoinhibitors. Reactive-site peptide-bond cleavage during inhibition could not be detected. Thus, the inhibitory behaviour is just as broad in specificity and as unusual as that of the trypsin-kallikrein inhibitor (Kunitz) from bovine organs. The N-terminus is blocked by pyroglutamic acid. Isoinhibitor K is the main component of the isoinhibitors secreted into the mucus and amounts to 35-40% of the mixture.

The acid-labile inter-alpha-trypsin inhibitor is cleaved enzymatically in vivo, liberating a smaller acid-stable inhibitor. The molar ratio of native inhibitor to this smaller inhibitor in plasma is significantly changed in some severe cases of inflammation and kidney injury. To clarify this observation on a molecular basis, the action of four different types of proteinases (trypsin, plasmin, kallikrein and granulocyte elastase) on the inter-alpha-trypsin inhibitor was studied. The initial rate of cleavage of the inter-alpha-trypsin inhibitor by a 1.3-fold molar excess of proteinase over inhibitor was found to be 4375 nM x min-1 with granulocyte elastase, 860 nM x min-1 with trypsin, 67 nM x min-1 with plasmin, and 0.3 nM X min-1 with kallikrein. Obviously, of the enzymes studied so far, the granulocyte elastase known to be released during severe inflammatory processes is by far the most potent proteinase in the transformation of the inter-alpha-trypsin inhibitor. The inter-alpha-trypsin inhibitor and its cleavage products inhibit bovine trypsin very strongly (Ki = 10(-9)--10(-11) M), porcine plasmin much less strongly, human plasmin very weakly and pancreatic kallikrein practically not at all.

Performic-acid-oxidized isoinhibitor K of snails (Helix pomatia) was subjected to arginine-directed tryptic proteolysis. Six peptide fragments including one overlap peptide from limited cleavage of the Arg-3-Pro-4 bond were purified to homogeneity. Four arginine peptides and the C-terminal peptide were sequenced by automatic Edman degradation using a special peptide program. The phenylthiohydantoins were all identified by chemical ionization mass spectrometry, except four cysteic acid residues that were identified on an amino acid analyzer after acid hydrolysis. Quantitative evaluation of the phenylthiohydantoins by chemical ionization mass spectrometry using total molecular-ion beam integration greatly facilitated sequencing. The mass spectrum of the dipeptide less than Glu-Gly revealed that the N-terminus was blocked by pyroglutamic acid. The complete amino acid sequence of isoinhibitor K was determined. An almost 50% homology between the sequences of the snail inhibitor and the bovine trypsin-kallikrein inhibitor (Kunitz) became obvious. A comparison of all homologous sequences of this particular class of proteins known to date is presented.

Reversible and selective modification of the guanidino group by 1,2-cyclohexanedione or 2,3-butanedione in borate buffer was applied to identify arginine residues in the reactive sites of proteinase inhibitors. The ability of the method to distinguish between arginine and lysine residues was examined. Trypsin inhibitors with arginine at the reactive site were almost completely inactivated within 2 h, e.g. the low-molecular weight inhibitors from soybeans (Kunitz), peanuts and porcine seminal plasma. Inhibitors of the lysine-type were not inactivated by 1,2-cyclohexanedione/borate, e.g. the bovine trypsin/kallikrein inhibitor, the trypsin inhibitors from cow colostrum, porcine pancreas, or snail epidermis (isoinhibitor K from Helix pomatia), and the human alpha1-proteinase inhibitor (alpha1-antitrypsin). However, 2,3-butanedione/borate does not show this high specificity. The method was applied to four high-molecular weight proteinase inhibitors from the albumin gland of the snail (Helix pomatia). All four inhibitors were subject to inactivation by the reagent, indicating an arginine residue at the reactive site. Evidence is given by NMR, UV, and titration data that a complex is formed from 1,2-cyclohexanedione and borate. Due to this complex formation, the amount of free carbonyl component is drastically decreased. Since 1,2-cyclohexanedione without borate lacks the high specificity for arginine residues, the borate complex of the reagent is presumed to be responsible for the high specificity. The new procedure for identification of reactive sites is based on a reversible modification of the guanidium group of the arginine residues.

Acidic extracts of washed, ejaculated human spermatozoa contain, besides acrosin, two proteinase inhibitors, a trypsin-chymotrypsin (elastase) inhibitor (HUSI-I) and a trypsin-acrosin inhibitor (HUSI-II). Using the indirect immunofluorescence technique these inhibitors could be localized in the spermatozoa. Ejaculated spermatozoa were treated with monospecific antibodies raised in rabbits against HUSI-I and HUSI-II, respectively, and with fluorescein-labeled IgG from goat directed against the rabbit IgG. If acetone-fixed spermatozoa were used, fluorescence appeared only in a small ring near or at the equatorial segment of the spermatozoa. After prefixation of washed spermatozoa with 0.36% formaldehyde, however, distribution of both inhibitors in the region of the acrosomal caps could clearly be demonstrated. Present results suggest that they are attached at the plasma membrane. Obviously, in the case of human spermatozoa the inhibitors are relatively easily detached together with the membrane so that prefixation is necessary to achieve proper localization.

The glandular kininogenase kallikrein is known to occur in many mammalian organs and glands but direct histochemical localization has been achieved in only a few cases. We have now been able to localize porcine kallikrein in the acinar cells of the pancreas and in the striated and collecting duct cells of the submandibular gland. Incubation of frozen and fixed sections with one of the crossreacting antibodies, anti-pancreatic, anti-submandibular or anti-urinary kallikrein IgG resulted in the same immunofluorescence pattern. There was evidence of a specific fluorescence neither in the acinar cells, nor in the interstitial tissue or blood cells of the submandibular gland nor in the islets of Langerhans, the interlobular ducts or blood vessels of the pancreas. From all data now available about glandular kallikreins, it seems that the kallikreins in these organs are very similar.

The newly synthesized chromogenic substrate D ValLeuArgNHNp was employed to study the inhibition strength of Trasylol-like inhibitors from bovine lung (TKI), sea anemone (SAI), snake venoms (NNV and HHV), snails (HPI) and cow colostrum (CTI) against porcine pancreatic, submandibular and urinary kallikreins. The dissociation constants of the corresponding kallikrein-inhibitor complexes were found close to Ki = 1.5 x 10(-9)M (TKI, SAI, NNV) or to Ki = 10--210 x 10(-9)M (HHV, HPI). CTI does not inhibit the three porcine glandular kallikreins. Comparison of the inhibitory active areas of the inhibitors with their affinities to the three kallikreins shows that kallikrein inhibition is observed only if basic amino acid residues are present in distinct positions of the inhibitory active sites.

Three ewes were vaccinated with boar sperm acrosin. Despite the presence of antiacrosin antibodies which crossreact with ram acrosin in the sera of the immunized sheep, no significant reduction in fertility was observed. Incubation of ejaculated or capacitated boar spermatozoa with anti-acrosin serum or IgG did not reduce the halos of digestion in the gelatinolysis test. However, an unexplained decrease of the forward progression and number of lytically active spermatozoa was observed after this treatment. We found antiacrosin antibodies and determined their titers in the sera of the vaccinated ewes, in colostrum and in aqueous extracts of cervix, uterus, oviduct and ovary. No antiacrosin antibodies could be detected in the sera of new born lambs. The immunoglobulins IgA, IgG and IgM were isolated from the sera of the ewes. The acrosin-specific antibodies belonged exclusively to the IgG class. In genital extracts the amount of IgG, IgA and IgM was determined. IgG was found in higher amount in every extract. IgA is present in similar amount only in the cervix, in the other parts only in traces. In all extracts IgM is found in a very low level. The specificity of the antibodies for acrosin was proven by active enzyme staining of the precipitin lines obtained by immunodiffusion.

Isoinhibitor K is the main component of the complex mixture of isoinhibitors of broad specificity secreted into the mucus by the Roman snail (Helix pomatia). The disulfide pairing was determined after the amino acid sequence had been elucidated. Two cystine-containing peptides with the disulfide bridges Cys32-Cys53 and Cys32-Cys53 plus Cys7-Cys57 were obtained after thermolytic hydrolysis of the native inhibitor at 80 degrees C and chromatographic separation of the peptides using SE-Sephadex. The Cys16-Cys40 disulfide bridge could be reduced selectively by sodium borohydride with no loss in biological activity. This property and the covalent structure correspond to that of the intracellular inhibitor from bovine organs, which is largely homologous in its amino acid sequence to the secretory inhibitor from the snail. The complete covalent structure of isoinhibitor K will be presented. The snail inhibitor is less stable against proteolytic inactivation by thermolysin and against thermal denaturation at pH 8.0 than the inhibitor from bovine organs (Kunitz inhibitor).